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Focus is on dogs with naturally-occurring primary hypoA which is thought to be due to immune-mediate destruction of the adrenal cortices.Adrenal cortices produce:

Glucocorticoids, especially cortisol. Cortisol is crucial for the normal function of a wide variety of organs and systems in the body including haemodynamics and the cardiovascular system, metabolism, inflammation and immunological function, and gastrointestinal integrity.

Most of the clinical findings in this disease can be attributed to deficiencies in these hormones.

Point 1 – “The Great Pretender”

Complex disease that can have a variable course affecting different dogs to a greater or lesser degree and presenting in a whole variety of ways with signs and findings that may be related to a number of organs or systems.Have a wide index of suspicion for hypoA and keep this disorder on your differential diagnosis list for a wide patient population.

Point 2 – Likely Genetic Basis

Genetic basis suspected based on epidemiological studies and pedigree analysisGenetic test for disease risk trying to be developed. Such a test would allow us to identify dogs at increased risk and enrol them into a screening programme. Furthermore, it could be used to inform breeding strategies and reduce the incidence of hypoA in susceptible dog breeds.Numerically diagnosed most often in crossbreed dogs but breeds known to be at increased risk include, but are not limited to:

Pont 3 – Aldosterone may be low in ‘atypical’ cases

Traditional term for Addisonian dogs presenting without electrolyte abnormalities – hyperkalaemia and/or hyponatraemiaThought to be due to glucocorticoid deficiency but adequate aldosterone level for time-being. But paper below reported low aldosterone levels even in ‘atypical’ cases. Why their plasma electrolyte levels remain within reference intervals remains unclear at this time.

At some point in the days, weeks or months after diagnosis they will develop electrolyte abnormalities and so they need to be monitored regularly for this.

Point 4 – Hypoglycaemia may be severe

When present hypoglycaemia in hypoA may range from mild to severe and can cause clinical signs including seizures.

Neuromuscular signs may occur in hypoA that are not due to hypoglycaemia

Dogs with exercise-induced episodic collapse may be Addisionian, may be suffering from another cause of hypoglycaemia, or may be hypoglycaemic Addisonians!

Point 5 – Bradycardia is not always present and not just due to hyperkalaemia

Be alert to a relative bradycardia, i.e. absence of compensatory tachycardia in a hypoperfused shocky dog; an inappropriately ‘normal’ heart rate.

Other factors that may act to slow the heart rate include:

Glucocorticoid deficiency; without enough cortisol the heart may not be able to respond to the positive chronotropic effects of endogenous catecholamines which is the compensatory response to hypovolaemia.

Cardiac hypoxia from hypoperfusion may be involved

Severe hypoglycaemia

High vagal tone due to many possible triggers

Point 6 – ACTH stimulation test provides definitive diagnosis

May be performed in-house in some practices nowadays using in-house cortisol analysers; also SNAP® Cortisol Test from Idexx,Validation, accuracy and reliability of in-house cortisol analysers?

Definitive diagnosis not needed before starting glucocorticoids if index of suspicion based on other clinical findings is sufficiently high.Dexamethasone can be used before test is performed/completed – only therapeutic corticosteroid that does not cross-react with the cortisol assay.

Point 7 – Single resting plasma cortisol may be useful for screening – but limited role in emergencies?

The following studies suggest that if a sick dog has plasma cortisol greater than 2 µg/dl (55 mmol/l) hypoA is very unlikely.On the flipside this diagnosis is very likely in a sick dog with plasma cortisol less than 1 µg/dl (28 mmol/l).A sick dog with plasma cortisol greater than 2 µg/dl (55 mmol/l) would be considered not to have the disease, a sick dog with plasma cortisol less than 2 µg/dl (55 mmol/l) would need an ACTH stimulation test performed to resolve this due to the poor predictive value of this test below this cut-off.Bear in mind that each reference laboratory and indeed in-house analyser will likely have its own cut-offs for resting cortisol.

Point 8 – Intravenous fluid therapy

First priority in stabilising Addisonian crisis using a bolus resuscitation strategy initially and then moving onto a lower rate infusionDebate about whether to use Hartmann’s, buffered lactated Ringer’s solution or Normosol-R in these patients or to use 0.9% sodium chloride – similar to considerations discussed HEREIn addition dogs with hypoA are typically hyponatraemic, most likely for some time. Rapid increase in plasma sodium may result in potentially irreversible and life-ending neurological complications.Plasma sodium concentration at presentation may therefore influence crystalloid choice. Avoid 0.9% sodium chloride if moderate-to-severe hyponatraemia present? Its sodium concentration is higher than the other fluids mentioned and this could increase risk of excessively fast correction of hyponatraemia.

Point 9 – Client communication and education

HypoA is a lifelong disorder that can be well managed but not cured and spontaneous resolution not reported.Clients need to be well-informed and fully on boardAlso need to be alert to periods of stress when dog may decompensate and prophylactic/therapeutic prednisolone needed

Point 10 – Prognosis is good with appropriate management – yey!

Reports suggest that natural death or euthanasia usually due to another non-related problem.But appropriate management is crucial!

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